Related Experiment Video

Updated: May 26, 2026

An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery
07:43

An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery

Published on: August 23, 2016

ERO1L Promotes NSCLC Invasion via ROS-Mediated EMT

Rui Xue1, Yahong Cai2, Guangzhen Bai1

  • 1Department of Thoracic Surgery, Zhuhai Hospital of Integrated Traditional Chinese and Western Medicine, Zhuhai, Guangdong, China.

Journal of Biochemical and Molecular Toxicology
|May 25, 2026
PubMed

Insights

ERO1L protein promotes non-small cell lung cancer (NSCLC) progression by increasing reactive oxygen species (ROS). Silencing ERO1L inhibits NSCLC cell invasion, migration, and proliferation, suggesting ERO1L as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality.
  • Understanding the molecular mechanisms driving NSCLC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of ERO1L (endoplasmic reticulum oxidoreductase 1-like) in NSCLC.
  • To explore the underlying molecular mechanisms, including reactive oxygen species (ROS) generation, epithelial-mesenchymal transition (EMT), and matrix metalloproteinase (MMP) expression.

Main Methods:

  • Lentivirus-mediated ERO1L silencing and overexpression in A549 NSCLC cells.
  • Assessment of cell migration, invasion, and proliferation.
  • Analysis of EMT markers, MMP expression, and intracellular ROS levels.
  • Utilization of N-acetylcysteine (NAC) as a ROS scavenger to confirm mechanism.

Main Results:

  • ERO1L was significantly upregulated in NSCLC tissues.
  • ERO1L silencing reduced ROS production, inhibited cell migration, invasion, and proliferation.
  • Silencing ERO1L reversed EMT and decreased MMP expression.
  • ERO1L overexpression yielded opposite effects.
  • NAC treatment partially reversed ERO1L-induced changes, confirming ROS dependence.

Conclusions:

  • ERO1L promotes NSCLC cell invasion, migration, and proliferation via a ROS-dependent mechanism.
  • This mechanism involves the regulation of EMT markers and MMP expression.
  • ERO1L represents a potential therapeutic target for NSCLC treatment.
Keywords:
ERO1LROSepithelial‐mesenchymal transitioninvasionmigrationnon‐small cell lung cancer

More Related Videos

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

Related Concept Videos

Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...